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[北京]清华大学医学院Charles David实验室2018招聘癌症生物学博士后

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清华大学医学院 Charles David实验室招聘癌症生物学博士后(2-3名) 时间:2018-01-03

大学医学院 Charles David实验室招聘癌症生物学博士后(2-3)

 

Charles David(戴超)实验具有清华北大联合中心的支持。实验室运用多种新实验手段定主宰癌症胞和组织胞命运的转录因子以及转录。研究定癌信号通路如何通挟持干胞的转录络诱导癌症

 

清华博士后享受有竞争力的待遇。实验室支持申博士后基金如CLS博士后基金、大学博士后支持划等.

 

招聘条件

1.具有分子和胞生物学, 生物化学, 或者癌症学相关专业博士学位,得博士学位2年以内;

2.3年以来,以第一作者身份在国知名学期刊发 (IF > 5) 研究文;

3.具有高的英写作及口交流能力.

 

材料及申方式

1个人简历 

2个人陈述 (研究背景,个人事业目标等;中英均可);

3两名推荐人的系方式。

将申材料至:cdavid@


 

Charles David’s Lab at Tsinghua University School of Medicine recruiting 2-3 postdoctoral fellows

 

The David laboratory is supported in part by the Peking-Tsinghua Center for Life Sciences (CLS). The laboratory uses cutting-edge approaches to parse essential tumorigenic transcriptional networks in cancer as well as the stem/progenitor cells that can serve as the cell of origin for neoplasms. The laboratory is also focused on understanding the specific molecular interactions between oncogenic signaling pathways and stem/progenitor-derived transcriptional networks.

 

Tsinghua University postdoctoral fellows enjoy competitive pay and benefits, and are able to apply for a wide range of additional support available at Tsinghua/CLS.

 

The successful candidate(s) will:

1. have a Ph.D. in the areas of molecular/cellular biology, biochemistry, epigenetics, or cancer biology within the last two years;

2. have published a first author paper in a reputable journal (IF > 5) in the past three years; AND

3. have proficiency in verbal and written English.

 

Applicants should supply:

1. an up-to-date CV;

2. a personal statement (detailing research experience, career goals etc.); AND

3. contact information for two references.

Please send application materials to: cdavid@mail.tsinghua.edu.

 

戴超代表成果如下:

 

1.David CJ, Huang YH, Chen M, Su J, Bardeesy N, Iacobuzio-Donahue CA, Massagué J (2016) TGF-β tumor suppression through a lethal EMT. Cell 164(5):1015-30.

2.David CJ, Boyne AB, Millhouse SR, Manley JL (2011). The RNA polymerase II C-terminal domain promotes splicing activation through recruitment of a U2AF65-Prp19 complex. Genes and Development 25: 972-83.

3.David CJ, Manley JL (2010). Alternative pre-mRNA splicing regulation in cancer: pathways and programs unhinged. Genes and Development 24: 2324-64.

4.David CJ*, Chen M*, Assanah M, Canoll P, Manley JL (2010). HnRNP proteins controlled by c-Myc deregulate pyruvate kinase mRNA splicing in cancer. Nature 463: 364-8.*Co-first author

5.David CJ, Manley JL (2008). The search for alternative splicing regulators: new approaches offer a path to a splicing code. Genes and Development 22: 279-85.